As the rate-limiting enzyme in polyamine biosynthesis, ODC1 is upregulated in macrophages in response to inflammatory stimuli and functions to attenuate the production of proinflammatory cytokines and inhibit ROS-induced apoptosis, suggesting a protective feedback mechanism.[48] Conversely, the loss of ODC1 promotes macrophage pyroptosis, a highly inflammatory form of cell death, exacerbating organ injury in septic models.[49] In GERD, dysregulated ODC1 could disrupt the delicate balance of mucosal repair and inflammatory responses in the esophageal epithelium. Here, ODC1 is linked to gastroesophageal reflux disease.